All-Potato Fat Busting Science

I'm going to post some interesting geek-speak on why the potato diet seems to be a very effective, fat burning tool. In the 'Eat MOAR Taters' thread http://www.marksdailyapple.com/forum/thread67137.html people have experienced a range of stellar weight loss to minimal, but at least no one ballooned up!

In the next couple posts, I will put up some of the science behind this, for your enjoyment...

"Eating 2-3000kcal/day of potatoes spikes blood glucose. The more potatoes you eat the more you spike glucose. The pancreas responds to hyperglycaemia by secreting insulin but also by upregulating pancreatic glucokinase production, which increases insulin secretion per unit rise in glucose. After a couple of days on an all potato diet your pancreas will be producing impressive amounts of post prandial insulin.

Insulin is degraded by insulin degrading enzyme. Very, very, very crudely (with a ton of qualifications, read the paper!) insulin action leads to insulin degradation. All insulin sensitive tissues degrade insulin. The liver is a massive sink for insulin, especially on a high carbohydrate diet. Anything which increases hepatic insulin sensitivity should increase hepatic insulin degradation. A sudden ceasation of free fatty acid supply from adipocytes will increase both hepatic insulin sensitivity and hepatic insulin degradation. A potato diet supplies relatively little in the way of fatty acids so there is also little dietary fat to supply the lipid intermediates to encourage hepatic insulin resistance.

Much of the hepatic uptake of glucose occurs without the direct intervention of insulin. The liver has large numbers of GLUT2s on its cells, which allow insulin-independent hepatic glucose uptake via a simple concentration gradient. The gradient is maintained by the intracellular phosphorylation of glucose, which allows its prompt removal to metabolism or storage as glycogen. Hepatic glucokinase does this phosphorylation and the production of the glucokinase enzyme in the liver is, of course, controlled by insulin. Increased insulin leads to increased glucokinase production and enhanced GLUT2 mediated glucose uptake.

Without fat, bulk calories are stored as glycogen, excepting that there is a little de novo fat synthesis from glucose in the liver. Hepatic glycogen does not cause hepatic insulin resistance. In the near absence of FFA supply the liver maintains insulin sensitivity and the ability to degrade insulin. Nothing like as much insulin reaches the periphery as is produced by the pancreas in response to 2-3000kcal of potatoes.

The second effect of shutting down free fatty acid supply from adipocytes and diet is the loss of fatty acid intermediates in muscle. Insulin sensitivity increases, the amount of insulin needed to facilitate glucose uptake by muscles decreases. Insulin secretion from the pancreas will then decrease but hepatic extraction of insulin continues while ever carbohydrate adaption continues.

The ultimate determinant of weight loss is fasting insulin. This determines how much lipolysis occurs during the period before the next meal. No one expects to lose weight during the 4 hours immediately after any meal. The following 8 hours, especially overnight, is when weight loss occurs.

Post absorptively, without dietary glucose input, there is no stimulus for anything other than basal insulin secretion. Fasting insulin will be low because muscles are insulin sensitive so relatively little insulin is needed for glucose uptake. As fasting insulin levels drop lipolysis will restart. Free fatty acids will feed back to the liver to cause some degree of hepatic insulin resistance, decrease first pass metabolism and stop too profound an hypoinsulinaemia occurring. But fat loss will happen.

So you have to ask whether an almost all potato diet genuinely leads low fasting insulin and subsequent weight loss. For my perspective the answer is yes. The precedent for this has to the Kitavans with fasting insulin levels of 4.0microIU/ml.

The next question is whether anyone could do this. That, I suspect, depends on how broken your liver is, ie is there irreversible hepatic insulin resistance. If you are overweight secondary to simple fatty liver, which is completely reversible, I suspect the answer is yes. If you have pathology in your liver such as NASH, especially with fibrosis, I think you might not respond in the same way. The more of a problem you have with obesity the less likely you are to lose weight or experience appetite normalisation (translates as access to adipose tissue calories). Ultimately the ability to live on varied macronutrient ratios comes down to how broken you are, especially your liver. Why a broken liver requires low carbohydrate eating is another post.

Is it healthy for someone with a functional liver to live on potatoes? It is clearly possible in the medium term. Cooked tubers have a respectable history of human usage. If you are not broken it might be a reasonable diet. There are no trans fats in spuds. There are minimal omega 6 fats. There is no gluten. There is just enough fructose to activate hepatic glucokinase without generating de novo lipogenesis. There is adequate high quality protein. On the down side there are a stack of vitamin and mineral deficiencies waiting in the wings.

I have no doubt that Chris Voight lost weight on an all potato diet. I also have no doubt that he was neither chronically hyperglycaemic nor hyperinsulinaemic.

There is no way of putting numbers to the framework with the data I have at the moment, but the physiology is comprehensible."

"How about scaling this up to a massive dose of potato induced insulin and limiting dietary fat? Severely limiting dietary fat. And never mind pussy footing around at 40g of mixed carbs and protein. There is a limit to how low FFAs can be driven, and it seems safe to assume that a baked potato or three might just inhibit lipolysis maximally and keep it that low for rather a long time. But if you deprive beta cells of free fatty acids you blunt their ability to secrete insulin. Very, very high carbohydrate diets really ought to be able to inhibit lipolysis to the point where the knock on effect is the inhibition of insulin secretion, provided you don't supply exogenous fat. Look at the nicotinic acid treated rats...

Once you get FFA levels low enough to inhibit insulin secretion you will start to move in to the sort of territory where insulin secretion might be blunted enough to allow hyperglycaemia. But the feedback effect of reduced insulin levels is also the re commencement of lipolysis. This will restore enough FFAs to maintain functional insulin secretion and so avoid potential hyperglycaemia, which the body tries to avoid. Of course you have to throw in the increased insulin sensitivity of muscles deprived of exogenously supplied FFAs too.

So is it possible to eat an ad lib, calorie unrestricted diet based on near pure carbohydrate and lose weight? Working from the premise that lowered insulin is a pre requisite for hunger free weight loss, as I always do, the answer is possibly yes. We all remember Chris Voight on his all potato diet (plus 20ml of olive oil, low in palmitate, per day) who lost a great deal of weight over a few weeks, the rate of weight loss accelerating as the weeks progressed? I had a think about it here, well before I had any inkling as to what might be happening in the electron transport chain."

Over the course of two months, Mr. Voigt lost 21 pounds. No one knows exactly how much of that weight came out of fat and how much out of lean mass, but the fact that he reported a decrease in waist and neck circumference indicates that most of it probably came out of fat. Previous long-term potato feeding experiments have indicated that it's possible to maintain an athletic muscle mass on the amount of protein in whole potatoes alone (4). So yes, Mr. Voigt lost fat on a very high-carbohydrate diet (75-80% carbohydrate, up to 440g per day).

On to the most interesting question: why did he lose fat? Losing fat requires that energy leaving the body exceed energy entering the body. But as Gary Taubes would say, that's obvious but it doesn't get us anywhere. In the first three weeks of his diet, Mr. Voigt estimates that he was only eating 1,600 calories per day. Aha! That's why he lost weight! Well, yes. But let's look into this more deeply. Mr. Voigt was not deliberately restricting his calorie intake at all, and he did not intend this as a weight loss diet. In my interview, I asked him if he was hungry during the diet. He said that he was not hungry, and that he ate to appetite during this period, realizing only after three weeks that he was not eating nearly enough calories to maintain his weight*. I also asked him how his energy level was, and he said repeatedly that it was very good, perhaps even better than usual. Those were not idle questions.

Calorie restriction causes a predictable physiological response in humans that includes hunger and decreased energy. It's the starvation response, and it's powerful in both lean and overweight people, as anyone knows who has tried to lose fat by decreasing calorie intake alone. The fact that he didn't experience hunger or fatigue implies that his body did not think it was starving. Why would that be?

"Starches are important as energy sources for humans and also for their interactions with the gut microflora throughout the digestive tact. Largely, those interactions promote human health. In the mouth, less gelatinised starches may lower risk of cariogensis. In the large bowel, starches which have escaped small intestinal digestion (resistant starch), together with proteins, other undigested carbohydrates and endogenous secretions are fermented by the resident microflora. The resulting short chain fatty acids contribute substantially to the normal physiological functions of the viscera. Specific types of resistant starch (e.g. the chemically modified starches used in the food industry) may be used to manipulate the gut bacteria and their products (including short chain fatty acids) so as to optimise health. In the upper gut, these starches may assist in the transport of probiotic organisms thus promoting the immune response and suppressing potential pathogens. However, it appears unlikely that current probiotic organisms can be used to modulate large bowel short chain fatty acids in adults although resistant starch and other prebiotics can do so. Suggestions that starch may exacerbate certain conditions (such as ulcerative colitis) through stimulating the growth of certain pathogenic organisms appear to be unfounded. Short chain fatty acids may modulate tissue levels and effects of growth factors in the gut and so modify gut development and risk of serious disease, including colo-rectal cancer. However, information on the relationship between starches and the microflora is relatively sparse and substantial opportunities exist both for basic research and food product development."

Starches and RS are emerging as important factors in health, especially through their interactions with gut bacteria. These interactions seem to occur both physically and through the metabolism of starches by the micro-organisms. It appears likely that starch fermentation in both the mouth and the large bowel can be modulated so as to lower disease risk. In the mouth, slower starch breakdown can reduce caries risk. In the colon, fermentation can promote SCFA production so as to optimise physiological function and manage and prevent important pathologies. It appears likely that the latter will involve tailoring the supply of RS to meet individual variations in the microflora which may limit starch fermentation. Newer varieties of starch high in RS are one of the means whereby this can be achieved. In this regard the parallels with NSP are striking. Dietary fibre used to be regarded as a single entity with multiple actions. Now, different NSP are known to affect gut physiology in disparate ways. The same appears to be true for RS1-4. Thus, identifying the factors which mean that the mix of bacteria in the microbial population which metabolise the various forms of RS appears to be an important research objective. Equally, identifying the ways in which the various types of RS can assist in delivering probiotics to the upper gut (to deal with infections) and to the large bowel (to optimise the microflora and to deliver SCFA) also is important. The relationships between the microflora in preweaned infants and those in adults, especially as influenced by starches seems to be important in promotion of gut health throughout life. The gaps in knowledge in these significant aspects of gut physiology are large and warrant exploration, especially as they relate to the gut microflora. Much of the technology (animal models, human faecal and in vitro measures, chemical and biological assays) is available to study microbial starch metabolism but the same cannot be said about the impact of starch on the microflora. While conventional culture and microscopic methods have provided the basic knowledge of the large bowel microlfora, they are limited both in scope and their demands for labour (Tannock, 1999). It is to be hoped that the application of new molecular methodologies will give a fuller understanding of the ways in which starches and other carbohydrates influence bacterial populations in the human gut.

You've almost just justified every arguement a low-fat/high carb vegan would ever be able to make against the paleo/primal diet.

Dagnabbit Otzi, stop giving them fuel!

Except for the fact that long-term application of this will crash and burn! I think the real answer to realistic dieting and great health is somewhere in the middle between hardcore paleo and hardcore vegan. I love Mark's Primal Blueprint...he allows for leeway into potatoes, sweet potatoes, etc... without the stigma of the paleo low-carb approach.

When Paleo villifies carbs and Vegans villify meat, there's no way you can thrive under the dogma you create. Open mindedness is where it's at. Insulin, gut health, etc... have to be part of the solution invariably.

Except for the fact that long-term application of this will crash and burn! I think the real answer to realistic dieting and great health is somewhere in the middle between hardcore paleo and hardcore vegan. I love Mark's Primal Blueprint...he allows for leeway into potatoes, sweet potatoes, etc... without the stigma of the paleo low-carb approach.

When Paleo villifies carbs and Vegans villify meat, there's no way you can thrive under the dogma you create. Open mindedness is where it's at. Insulin, gut health, etc... have to be part of the solution invariably.

Perhaps, but don't expect a hardcore vegan paleo-basher to take that kind of balanced approach. They'll just take info like this and spread it like the gospel.

"Diet-induced obesity depends not just on calories ingested but also on the host's microbiome," said the study's senior author Yang-Xin Fu, MD, PhD, professor of pathology at the University of Chicago Medicine. For most people, he said, "host digestion is not completely efficient, but changes in the gut flora can raise or lower digestive efficiency."

So the old adage "you are what you eat" needs to be modified, Fu suggested, to include, "as processed by the microbial community of the distal gut and as regulated by the immune system."